Patients with rheumatoid arthritis (RA) are known to have an increased risk for cardiovascular events, with chronic inflammation implicated in the development of myocardial dysfunction. Myocardial abnormalities on cardiac MRI (cMRI) have been previously reported in patients with active RA.
In this cardiac follow-up study, data were collected from 58 female patients with active RA from 2 subgroups—those with untreated early RA (ERA; n = 30) and chronic RA (CRA; n = 28), 22 sex- and age-matched patients with fibromyalgia (FM), and 35 healthy volunteers. The ERA cohort included patients starting conventional synthetic disease-modifying antirheumatic drugs (csDMARDs; n = 28) or biological DMARDs (bDMARDs; n = 2), whereas all patients in the CRA cohort received bDMARDs. Patients with coronary artery disease and/or diabetes, along with smokers and the elderly (aged >70 years), were excluded. All RA patients underwent cMRI before and after 1 year of DMARD therapy; sex- and age-matched FM patients and healthy volunteers underwent cMRI once. cMRI (1.5T or 3T) included analyses of T1 relaxation times, late gadolinium enhancement (LGE), and cardiac functions.
The baseline characteristics of the RA and FM cohorts were largely similar, but the FM cohort had higher cardiovascular (CV) risk factors overall, including body mass index, waist circumference, HbA1c, low-density lipoprotein, and serum uric acid levels. In the ERA cohort, 83% received combination therapy at baseline that was ongoing at 1 year of follow-up; 86% of CRA patients received anti–tumor necrosis factor therapy and half had received csDMARD combinations at baseline. In both the ERA and CRA groups, significant decline in Disease Activity Score 28-joint count C-reactive protein was noted in the ERA group (mean + standard deviation [SD]: 3.7 + 1.0 vs 2.0 + 1.0; P <.001) and in the CRA group (mean + SD: 3.3 + 1.1 vs 2.6 + 0.9; P = .002).
Patients with active RA showed several myocardial abnormalities on cMRI at baseline—LGE, prolonged myocardial T1 relaxation times, and impaired cardiac function. In contrast to FM patients who showed no LGE, RA patients showed frequent LGE both at baseline (67%) and at follow-up (66%), indicating myocardial scars. Prolonged myocardial T1 relaxation times at baseline were reported in RA patients versus FM patients (1.5T cMRI, mean + SD: 1038 ± 90 vs 1010 ± 37 ms; 3.0T cMRI, mean + SD: 1125 ± 80 vs 1068 ± 123 ms), suggesting diffuse inflammation or fibrosis. T1 relaxation time only improved in patients with CRA.
Myocardial function was also impaired in RA patients at baseline compared with FM patients or healthy volunteers. However, findings from cardiac magnetic resonance showed that a significant improvement in cardiac function was observed in RA patients over the study period (right ventricle end-systolic volume, mean + SD: baseline, 36 + 8 mL/m2; follow-up, 34 + 7 mL/m2; P = .043) and in left-ventricle time to peak filling rate (mean + SD: 496 + 96 ms vs 445 + 126 ms; P = .010); no significant improvements in cardiac functions were noted in the CRA cohort.
These results were consistent with previous reports that patients with active RA show myocardial abnormalities on cMRI at baseline compared with FM controls despite having higher CV risk factors. Significant improvements in myocardial function were achieved by patients with early RA concomitant with decreasing RA activity following active treatment for 1 year, suggesting that tight control of RA activity may improve myocardial function.
Leirisalo-Repo M, et al. ACR 2017. Abstract 872.